The Mi{ET1} element in Mi{ET1}CsasMB04236 has been excised, resulting in a 431b deletion removing the start codon and two exons encoding the N-terminal part of Csas required for the enzymatic activity of CMP-Sia synthetases.
A 431 bp deletion resulting from the imprecise excision of Mi{ET1}CsasMB04236, which extends from the insertion site and removes the first two exons of the gene.
CsasMB04236 mutant flies are paralysed at elevated temperatures. No paralysis is detected in heterozygotes.
CsasMB04236/Csas21 mutant flies are paralysed at elevated temperatures.
No significant difference is detected in the resting membrane potential of muscle cells between Csas21 mutant and wild type larvae. Evoked Excitatory Junctional Potential (EJP) amplitude is reduced in Csas21 mutant larvae compared to wild type.
Csas21 has paralytic | adult stage | recessive phenotype, enhanceable by SiaTL22
Csas21 has abnormal neurophysiology | larval stage phenotype, non-enhanceable by SiaTL22
Csas21 has paralytic | adult stage | recessive phenotype, non-enhanceable by ST6Gal[+]/SiaTL22
Csas21 is an enhancer of paralytic | adult stage | recessive phenotype of SiaTL22
Csas21/Csas[+] is a non-enhancer of paralytic | adult stage | recessive phenotype of SiaTL22
Homozygous ST6GalL22 enhances the paralysis defect seen in Csas21 mutant flies at elevated temperatures. The time of onset of paralysis is shorter than in either Csas21 or ST6GalL22 mutants alone. One copy of ST6GalL22 does not enhance the homozygous Csas21 phenotype, and one copy of Csas21 is insufficient to enhance the ST6GalL22 mutant phenotype.
Homozygous Csas21 enhances the reduction in EJP amplitude seen in homozygous ST6GalL22 mutant flies, producing a EJP similar in magnitude to that seen in homozygous Csas21 mutant flies.
